scholarly journals   The effect of risk elements in soil to nitric oxide metabolism in tobacco plants

2012 ◽  
Vol 58 (No. 10) ◽  
pp. 435-440 ◽  
Author(s):  
D. Procházková ◽  
D. Haisel ◽  
D. Pavlíková ◽  
R. Schnablová ◽  
J. Száková ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Nitrogen Species ◽  
Nitrosative Stress ◽  
Photochemical Efficiency ◽  
Stability Index ◽  
No Production ◽  
Oxide Content ◽  
Risk Elements ◽  
Nitric Oxide Metabolism ◽  
Endogenous Nitric Oxide

We studied changes of endogenous nitric oxide content (NO) and of reactive nitrogen species metabolism in transgenic tobacco with prolonged life span (SAG) and in wild tobacco (WT) cultivated in the control and in the polluted soil. There was no difference in the metal accumulation between WT and SAG plants however SAG ones showed better ability to cope with risk elements, as they retained higher membrane stability index and chlorophyll content together with better photochemical efficiency and lower deepoxidation status. Risk elements induced higher NO production in the youngest leaves of both plant types. Low and middle leaves of both WT and SAG plants showed similar activities of nitrate reductase and nitrosoglutathione reductase. Increase of nitrotyrosine content in leaf soluble proteins suggests that risk elements induced nitrosative stress in both plant types.

The content of nitric oxide and S-nitrosothiols in rats’ liver cells under the different supplementation of macronutrient

2020 ◽  
Vol 12 (2) ◽  
pp. 187-195
Author(s):  
Halyna Kopylchuk ◽  
Ivanna Nykolaichuk ◽  
Olesiia Kuziak
Keyword(s):  
Nitric Oxide ◽  
Nitrogen Oxide ◽  
Nitrosative Stress ◽  
Liver Cells ◽  
Oxide Content ◽  
Experimental Conditions ◽  
Before And After ◽  
Rat Liver Cells ◽  
Key Factor ◽  
Excessive Consumption

This paper presents studies of nitric oxide and low-molecular S-nitrosothiols in the mitochondrial and cytosolic fractions of the rats' liver under the conditions of, alimentary protein deprivation, consumption of excess sucrose content and combined action of two adverse factors. In order to model the low-protein diet of the animal for 28 days received an isocaloric diet containing 4.7% protein, 10% fat, 81,3% carbohydrates (starch – 37%, sucrose – 30%, cellulose – 5%) and was calculated in accordance with the recommendations of the American Institute of Nutrition. The high-sugar diet consisted of 14% protein, 10% fat, 72% carbohydrates (starch – 37%, sucrose – 30%, cellulose – 5%). The mitochondrial and cytosolic fraction of rat liver cells were obtained by the method of differential centrifugation. Nitrogen oxide content was assessed by a unified method by determining the NO2- content, which is a stable metabolite of nitric oxide. Since NO is inactivated into an oxidase reaction with the conversion into nitrite or nitrate that is quickly metabolized, the nitrogen oxide content was assessed by the change in NO2-. The concentration of S-nitrosothiols was recorded, respectively, by determining the concentration of nitrite anion before and after the addition of Hg2+ ions, which by modifying the S – N bonds catalyzes the release of S-nitrosyl thiols of nitric oxide. An increase in NO content in both hepatic subcellular fractions of the rats’ experimental groups compared to control values was found. However, a lack of protein in the diet (protein deficiency in the diet leads to an increase in nitric oxide levels in 3-4 times) can be considered as a key factor in the recorded changes in the mitochondria of the animals’ liver, while in the cytosol - excessive consumption of sucrose (3-5 times increase). Regarding the level of S-nitrosothiols, in the studied fractions, multidirectional changes in their concentration were found. Thus, an increase in the content of nitrosyl derivatives in the mitochondria of rat’s liver cells with a simultaneous decrease in their level in the cytosol indicates dysmetabolic disorders in the transport system and deposition of nitric oxide, which can lead to the development of nitrosative stress under the experimental conditions.

Role of endogenous nitric oxide in endotoxin-induced alteration of hypoxic pulmonary vasoconstriction in mice

2005 ◽  
Vol 289 (2) ◽  
pp. H823-H831 ◽  
Author(s):  
Fabian Spöhr ◽  
Annemiek J. M. Cornelissen ◽  
Cornelius Busch ◽  
Martha M. Gebhard ◽  
Johann Motsch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
No Production ◽  
Wild Type ◽  
Pulmonary Vasodilation ◽  
Congenital Deficiency ◽  
Pulmonary Vasoconstriction ◽  
Vasoconstrictor Response ◽  
Endogenous Nitric Oxide ◽  
Deficient Mice

Pulmonary vasoconstriction in response to alveolar hypoxia (HPV) is frequently impaired in patients with sepsis or acute respiratory distress syndrome or in animal models of endotoxemia. Pulmonary vasodilation due to overproduction of nitric oxide (NO) by NO synthase 2 (NOS2) may be responsible for this impaired HPV after administration of endotoxin (LPS). We investigated the effects of acute nonspecific ( NG-nitro-l-arginine methyl ester, l-NAME) and NOS2-specific [l- N6-(1-iminoethyl)lysine, l-NIL] NOS inhibition and congenital deficiency of NOS2 on impaired HPV during endotoxemia. The pulmonary vasoconstrictor response and pulmonary vascular pressure-flow (P-Q) relationship during normoxia and hypoxia were studied in isolated, perfused, and ventilated lungs from LPS-pretreated and untreated wild-type and NOS2-deficient mice with and without l-NAME or l-NIL added to the perfusate. Compared with lungs from untreated mice, lungs from LPS-challenged wild-type mice constricted less in response to hypoxia (69 ± 17 vs. 3 ± 7%, respectively, P < 0.001). Perfusion with l-NAME or l-NIL restored this blunted HPV response only in part. In contrast, LPS administration did not impair the vasoconstrictor response to hypoxia in NOS2-deficient mice. Analysis of the pulmonary vascular P-Q relationship suggested that the HPV response may consist of different components that are specifically NOS isoform modulated in untreated and LPS-treated mice. These results demonstrate in a murine model of endotoxemia that NOS2-derived NO production is critical for LPS-mediated development of impaired HPV. Furthermore, impaired HPV during endotoxemia may be at least in part mediated by mechanisms other than simply pulmonary vasodilation by NOS2-derived NO overproduction.

scholarly journals Increased iNOS and Nitrosative Stress in Dopaminergic Neurons of MDMA-Exposed Rats

2019 ◽  
Vol 20 (5) ◽  
pp. 1242 ◽  
Author(s):  
Stefania Schiavone ◽  
Margherita Neri ◽  
Angela Maffione ◽  
Paolo Frisoni ◽  
Maria Morgese ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dopaminergic Neurons ◽  
Reactive Nitrogen Species ◽  
Nitrosative Stress ◽  
Inos Expression ◽  
Oxygen Species ◽  
Nitrogen Species ◽  
Neuronal Nuclei ◽  
Enzymatic Systems ◽  
The Brain

Several mechanisms underlying 3,4-Methylenedioxy-N-methylamphetamine (MDMA) neurotoxicity have been proposed, including neurochemical alterations and excitotoxicity mediated by reactive oxygen species (ROS), nitric oxide (NO), and reactive nitrogen species (RNS). However, ROS, NO, and RNS sources in the brain are not fully known. We aimed to investigate possible alterations in the expression of the ROS producer NOX enzymes (NOX2, NOX1, and NOX4), NO generators (iNOS, eNOS, and nNOS), markers of oxidative (8-hydroxy-2′-deoxyguanosine, 8OHdG), and nitrosative (3-nitrotyrosine, NT) stress, as well as the colocalization between cells positive for the dopamine transporter (DT1) and cells expressing the neuronal nuclei (NeuN) marker, in the frontal cortex of rats receiving saline or MDMA, sacrificed 6 h, 16 h, or 24 h after its administration. MDMA did not affect NOX2, NOX1, and NOX4 immunoreactivity, whereas iNOS expression was enhanced. The number of NT-positive cells was increased in MDMA-exposed animals, whereas no differences were detected in 8OHdG expression among experimental groups. MDMA and NT markers colocalized with DT1 positive cells. DT1 immunostaining was found in NeuN-positive stained cells. Virtually no colocalization was observed with microglia and astrocytes. Moreover, MDMA immunostaining was not found in NOX2-positive cells. Our results suggest that iNOS-derived nitrosative stress, but not NOX enzymes, may have a crucial role in the pathogenesis of MDMA-induced neurotoxicity, highlighting the specificity of different enzymatic systems in the development of neuropathological alterations induced by the abuse of this psychoactive compound.

scholarly journals Nitric Oxide Metabolism in Neisseria meningitidis

2002 ◽  
Vol 184 (11) ◽  
pp. 2987-2993 ◽  
Author(s):  
Muna F. Anjum ◽  
Tânia M. Stevanin ◽  
Robert C. Read ◽  
James W. B. Moir
Keyword(s):  
Nitric Oxide ◽  
Nitrous Oxide ◽  
Neisseria Meningitidis ◽  
Gene Product ◽  
Meningococcal Disease ◽  
Nitrite Reductase ◽  
Nitrosative Stress ◽  
Anaerobic Growth ◽  
Gene Products ◽  
Nitric Oxide Metabolism

ABSTRACT Neisseria meningitidis, the causative agent of meningococcal disease in humans, is likely to be exposed to nitrosative stress during natural colonization and disease. The genome of N. meningitidis includes the genes aniA and norB, predicted to encode nitrite reductase and nitric oxide (NO) reductase, respectively. These gene products should allow the bacterium to denitrify nitrite to nitrous oxide. We show that N. meningitidis can support growth microaerobically by the denitrification of nitrite via NO and that norB is required for anaerobic growth with nitrite. NorB and, to a lesser extent, the cycP gene product cytochrome c′ are able to counteract toxicity due to exogenously added NO. Expression of these genes by N. meningitidis during colonization and disease may confer protection against exogenous or endogenous nitrosative stress.

scholarly journals Nitric Oxide-Mediated Posttranslational Modifications: Impacts at the Synapse

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Sophie A. Bradley ◽  
Joern R. Steinert
Keyword(s):  
Nitric Oxide ◽  
Synaptic Transmission ◽  
Posttranslational Modifications ◽  
Nitrosative Stress ◽  
Long Term Potentiation ◽  
No Production ◽  
Normal Brain ◽  
Calcium Dependent ◽  
Physiological Processes

Nitric oxide (NO) is an important gasotransmitter molecule that is involved in numerous physiological processes throughout the nervous system. In addition to its involvement in physiological plasticity processes (long-term potentiation, LTP; long-term depression, LTD) which can include NMDAR-mediated calcium-dependent activation of neuronal nitric oxide synthase (nNOS), new insights into physiological and pathological consequences of nitrergic signalling have recently emerged. In addition to the canonical cGMP-mediated signalling, NO is also implicated in numerous pathways involving posttranslational modifications. In this review we discuss the multiple effects of S-nitrosylation and 3-nitrotyrosination on proteins with potential modulation of function but limit the analyses to signalling involved in synaptic transmission and vesicular release. Here, crucial proteins which mediate synaptic transmission can undergo posttranslational modifications with either pre- or postsynaptic origin. During normal brain function, both pathways serve as important cellular signalling cascades that modulate a diverse array of physiological processes, including synaptic plasticity, transcriptional activity, and neuronal survival. In contrast, evidence suggests that aging and disease can induce nitrosative stressviaexcessive NO production. Consequently, uncontrolled S-nitrosylation/3-nitrotyrosination can occur and represent pathological features that contribute to the onset and progression of various neurodegenerative diseases, including Parkinson’s, Alzheimer’s, and Huntington’s.

Caloric restriction increases free radicals and inducible nitric oxide synthase expression in mice infected with Salmonella Typhimurium

2011 ◽  
Vol 31 (4) ◽  
pp. 273-282 ◽  
Author(s):  
José Trujillo-Ferrara ◽  
Rafael Campos-Rodríguez ◽  
Eleazar Lara-Padilla ◽  
Daniel Ramírez-Rosales ◽  
José Correa Basurto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Free Radicals ◽  
Nitric Oxide Synthase ◽  
Salmonella Typhimurium ◽  
Caloric Restriction ◽  
Host Response ◽  
No Production ◽  
Oxide Content ◽  
Iron Nitrosyl ◽  
Oxide Synthase

It is well known that CR (caloric restriction) reduces oxidative damage to proteins, lipids and DNA, although the underlying mechanism is unclear. However, information concerning the effect of CR on the host response to infection is sparse. In this study, 6-month-old mice that were fed AL (ad libitum) or with a CR diet were infected with Salmonella serovar Typhimurium. EPR (electron paramagnetic resonance; also known as ESR (electron spin resonance)) was used to identify FRs (free radicals). These results were subsequently correlated with SOD (superoxide dismutase) catalytic activity, iNOS [inducible NOS (nitric oxide synthase) or NOSII] expression and NO (nitric oxide) content. EPR analysis of liver samples demonstrated that there was a higher quantity of FRs and iron–nitrosyl complex in infected mice provided with a CR diet as compared with those on an AL diet, indicating that CR was beneficial by increasing the host response to Salmonella Typhimurium. Furthermore, in infected mice on the CR diet, NOSII expression was higher, NO content was greater and spleen colonization was lower, compared with mice on the AL diet. No changes in SOD activity were detected, indicating that the NO produced participated more in the formation of iron–nitrosyl complexes than peroxynitrite. These results suggest that CR exerts a protective effect against Salmonella Typhimurium infection by increasing NO production.

scholarly journals Identification ofHistoplasma capsulatumTranscripts Induced in Response to Reactive Nitrogen Species

2005 ◽  
Vol 16 (10) ◽  
pp. 4792-4813 ◽  
Author(s):  
M. Paige Nittler ◽  
Davina Hocking-Murray ◽  
Catherine K. Foo ◽  
Anita Sil
Keyword(s):  
Nitric Oxide ◽  
Reactive Nitrogen Species ◽  
Nitrosative Stress ◽  
Histoplasma Capsulatum ◽  
Iron Acquisition ◽  
Pathogenic Fungus ◽  
Ectopic Expression ◽  
Open Reading Frames ◽  
Reactive Nitrogen ◽  
Nitrogen Species

The pathogenic fungus Histoplasma capsulatum escapes innate immune defenses and colonizes host macrophages during infection. After the onset of adaptive immunity, the production of the antimicrobial effector nitric oxide (.NO) restricts H. capsulatum replication. However, H. capsulatum can establish persistent infections, indicating that it survives in the host despite exposure to reactive nitrogen species (RNS). To understand how H. capsulatum responds to RNS, we determined the transcriptional profile of H. capsulatum to.NO-generating compounds using a shotgun genomic microarray. We identified 695 microarray clones that were induced ≥4-fold upon nitrosative stress. Because our microarray clones were generated from random fragments of genomic DNA, they did not necessarily correspond to H. capsulatum open reading frames. To identify induced genes, we used high-density oligonucleotide tiling arrays to determine the genomic boundaries and coding strand of 153 RNS-induced transcripts. Homologues of these genes in other organisms are involved in iron acquisition, energy production, stress response, protein folding/degradation, DNA repair, and.NO detoxification. Ectopic expression of one of these genes, a P450 nitric oxide reductase homologue, was sufficient to increase resistance of H. capsulatum to RNS in culture. We propose that H. capsulatum uses the pathways identified here to cope with RNS-induced damage during pathogenesis.

scholarly journals Nitric Oxide as a Target for Phytochemicals in Anti-Neuroinflammatory Prevention Therapy

2021 ◽  
Vol 22 (9) ◽  
pp. 4771
Author(s):  
Lalita Subedi ◽  
Bhakta Prasad Gaire ◽  
Amna Parveen ◽  
Sun-Yeou Kim
Keyword(s):  
Nitric Oxide ◽  
Neurological Disorders ◽  
Reactive Nitrogen Species ◽  
Therapeutic Strategy ◽  
No Production ◽  
Inflammatory Signaling ◽  
Cns Disorders ◽  
Prevention Therapy ◽  
The Central Nervous System ◽  
Lateral Sclerosis

Nitric oxide (NO) is a neurotransmitter that mediates the activation and inhibition of inflammatory cascades. Even though physiological NO is required for defense against various pathogens, excessive NO can trigger inflammatory signaling and cell death through reactive nitrogen species-induced oxidative stress. Excessive NO production by activated microglial cells is specifically associated with neuroinflammatory and neurodegenerative conditions, such as Alzheimer’s and Parkinson’s disease, amyotrophic lateral sclerosis, ischemia, hypoxia, multiple sclerosis, and other afflictions of the central nervous system (CNS). Therefore, controlling excessive NO production is a desirable therapeutic strategy for managing various neuroinflammatory disorders. Recently, phytochemicals have attracted considerable attention because of their potential to counteract excessive NO production in CNS disorders. Moreover, phytochemicals and nutraceuticals are typically safe and effective. In this review, we discuss the mechanisms of NO production and its involvement in various neurological disorders, and we revisit a number of recently identified phytochemicals which may act as NO inhibitors. This review may help identify novel potent anti-inflammatory agents that can downregulate NO, specifically during neuroinflammation and neurodegeneration.

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